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At least 613 records · Page 34Linked to original sources
PubMed2005

Pulmonary function after complete unilateral phrenic nerve transection.

OBJECT: The status of pulmonary function following phrenic nerve transfer surgery is still largely unknown because of the high degree of variability in the accessory phrenic nerve that may be involved. In the present study, pulmonary functions were assessed in patients before and after full-length phrenic nerve transfer surgery, in whom the phrenic nerve was severed at a location just before its entry into the diaphragm. METHODS: Fifteen patients (average age 27.4 years) with complete brachial plexus palsy underwent full-length phrenic nerve transfer. The phrenic nerve was harvested from the thoracic cavity by means of video-assisted thoracic surgery and then transferred to the musculocutaneous nerve. Postoperative pulmonary functions were retrospectively analyzed. Patients underwent follow-up evaluation for 42 to 48 months; four patients were eventually lost to follow up. Although no patient experienced pulmonary problems following the surgery, all sustained varying degrees of diaphragmatic paralysis and elevation (for 1-1.5 intercostal spaces) on the surgically treated side as seen on chest x-ray films. Pulmonary functional parameters, including vital capacity, vital capacity in percentage of predicted values, residual volume, total lung capacity, forced vital capacity, and forced expiratory volume in 1 second, recovered to preoperative levels by 1 year postsurgery. In contrast, the postoperative maximal inspiratory pressure value was significantly decreased compared with the predicted values (average decrease approximately 20%) in all of the patients, even at 4 years after the surgery. CONCLUSIONS: In young patients with healthy lung function, unilateral phrenic nerve transection surgery can cause unilateral diaphragmatic paralysis and reduce the inspiration muscle force; however, most pulmonary function parameters gradually recover to preoperative levels within 1 year.

Adolescent↗
PubMed1998

Controlled ethyl tert-butyl ether (ETBE) exposure of male volunteers. II. Acute effects.

The aim of this study was to evaluate acute effects of ethyl tert-butyl ether (ETBE) in man after short-term exposure. ETBE may in the future replace methyl tert-butyl ether, a widely used oxygenate in unleaded gasoline. Eight healthy male volunteers were exposed to ETBE vapor for 2 h at four levels (0, 5, 25, and 50 ppm) during light physical exercise. The subjects rated irritative symptoms, discomfort, and central nervous system effects in a questionnaire. Ocular (eye redness, tear film break-up time, conjunctival epithelial damage, and blinking frequency), nasal (acoustic rhinometry and analysis of inflammatory markers and cells in nasal lavage fluid), and pulmonary (peak expiratory flow, forced expiratory volume in 1 s, forced vital capacity, vital capacity, and transfer factor) measurements were performed. Significantly increased ratings of solvent smell (p = 0.001, repeated-measures ANOVA) were seen during exposures and correlated to exposure levels. Furthermore, significantly elevated ratings of discomfort in throat and airways were seen during and after 50 ppm compared to the control exposure (p = 0.02). Increased nasal swelling (p = 0.001) and blinking frequency (p = 0.01) were noted at all exposure levels, but their magnitudes were not related to exposure levels. A slightly impaired pulmonary function was seen at 25 and 50 ppm, since forced vital capacity (p = 0.02) and vital capacity (p = 0.04) differed significantly from the clean air exposure. Although the impairments seemed to fall within normal inter- and intraindividual variation and have no clinical relevance as such, it cannot be excluded that other individuals may react more severely than eight healthy male volunteers in this study.

Administration, Inhalation↗
PubMed1995

Pulmonary function alterations after 3 wk of exposure to hypobaria and/or hypoxia in growing rats.

We studied lung growth in rats between 4 and 7 wk of age under different conditions. There were five groups, seven animals in each: 1) general controls (ambient pressure and room air, food ad libitum); 2) hypobaric normoxic [barometric pressure (PB) 410 mmHg, PO2 153 Torr]; 3) normobaric hypoxic (ambient pressure, PO2 80 Torr); 4) hypobaric hypoxic (PB 410 mmHg, PO2 80 Torr); and 5) weight-matched controls to hypobaric hypoxic. Residual volume, functional residual capacity, vital capacity, and total lung capacity grew 10-20% more in both hypoxic groups than in weight-matched and general controls. Expiratory flow rates corrected for forced vital capacity decreased, and specific airway resistance increased significantly. In addition, the ratio of forced expiratory volume in 0.1 s to %forced vital capacity, peak expiratory flow rate, and forced maximal midexpiratory flow were also lower in normobaric hypoxic animals compared with weight-matched controls. Above a transpulmonary pressure of 6 cmH2O, flows were reduced in both hypoxic groups. No differences were observed between hypobaric normoxic and general control groups for lung volume and lung function. In weight-matched animals, total lung capacity decreased but lung function remained unchanged. We conclude that accelerated lung growth in hypobaric hypoxia and normobaric hypoxia is dysanaptic. Lung growth in hypobaric hypoxia is primarily induced by low oxygen, but differences between hypobaric hypoxia and normobaric hypoxia suggest a beneficial effect of low pressure.

Animals↗
PubMed1980

Abnormalities in maximum flow volume curve and closing volume in patients with hepatic cirrhosis.

Pulmonary functions were measured in 53 patients with hepatic cirrhosis in whom there was no clinical or radiographic evidence of pulmonary involvement. Spirometric tests such as total lung capacity, vital capacity, functional residual capacity, residual volume and forced expiratory volume during one second were within normal ranges, in all subjects. Flow volume curve and closing volume tests, however, were abnormal in the majority. The maximal expiratory flow at 50 per cent of vital capacity was not altered but the maximal expiratory flow at 25 percent of vital capacity was decreased significantly in patients with hepatic cirrhosis. The closing volume in patients with hepatic cirrhosis was also significantly increased. The abnormalities in flow volume curve and closing volume curve were also demonstrated in non-smokers, and at any age, in cases of hepatic cirrhosis. These results suggested that the narrowing or closure in small airways may occur in patients with hepatic cirrhosis. These changes may be due to mechanical compression of small airways but interstitial edema which was induced by presence in the circulating blood of vasoactive substances and endotoxins.

Adult↗